Abstract
A collateral sensitivity or a very modest cross-resistance to BBR 3464 was found in 2 ovarian cancer cell lines with experimentally induced resistance to cisplatin. Loss of mismatch repair proteins (hMLH1, hPMS2) or overexpression of nucleotide excision repair proteins (ERCC1) was not detrimental for the cellular sensitivity to BBR 3464. Moreover, interesting differences in the kinetics of formation and removal of DNA lesions at the single-gene (N- ras) level were observed between BBR 3464 and CDDP.
MeSH Terms
Adaptor Proteins, Signal Transducing
Adenosine Triphosphatases
Antineoplastic Agents/toxicity
Base Pair Mismatch
Carrier Proteins
Cell Survival/drug effects
Cisplatin/toxicity
DNA Repair/drug effects,genetics
DNA Repair Enzymes
DNA-Binding Proteins
Drug Resistance, Neoplasm
Endonucleases
Female
Humans
Mismatch Repair Endonuclease PMS2
MutL Protein Homolog 1
Neoplasm Proteins/genetics
Nuclear Proteins
Organoplatinum Compounds/toxicity
Ovarian Neoplasms
Polymerase Chain Reaction
Proteins/genetics
Tumor Cells, Cultured
Chemicals
Adaptor Proteins, Signal Transducing
Antineoplastic Agents
Carrier Proteins
DNA-Binding Proteins
MLH1 protein, human
Neoplasm Proteins
Nuclear Proteins
Organoplatinum Compounds
Proteins
ERCC1 protein, human
Endonucleases
Adenosine Triphosphatases
PMS2 protein, human
Mismatch Repair Endonuclease PMS2
MutL Protein Homolog 1
DNA Repair Enzymes
BBR 3464
Cisplatin
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Colella G
Department of Experimental Oncology, Istituto Nazionale per lo Studio e la Cura dei Tumori, Via Venezian 1, 20133 Milan, Italy.
Pennati M
Bearzatto A
Leone R
Colangelo D
Manzotti C
Daidone M G
Zaffaroni N